International Medical Department, China-Japan Friendship Hospital, Beijing, 100029, People's Republic of China.
In Vitro Cell Dev Biol Anim. 2019 Dec;55(10):793-800. doi: 10.1007/s11626-019-00399-4. Epub 2019 Aug 23.
MicroRNAs (miRNAs) are recognized to hold essential parts in the course of pathophysiology participating in myocardial ischemia/reperfusion (I/R) injury. The current study was intended to appraise the functional implication and underlying regulatory mechanism action of miR-20a in myocardial I/R injury. In cardiomyocyte hypoxia/reoxygenation (H/R) model simulating I/R, we observed that miR-20a was diminished in H9c2 cells subjected to H/R. The miR-20a mimics promoted cardiomyocyte viability and reduced H/R-triggered cell apoptosis, while the miR-20a inhibitors induced the inverse response in H9c2 cells subjected to H/R injury. Moreover, we ascertained that TLR4 was one downstream target gene of miR-20a and revealed that miR-20a might hold its protective action on cardiomyocytes subjected to H/R by inactivating p38 MAPK/JNK signaling. In summary, this study highlighted the relieved potential of miR-20a against cardiomyocyte H/R injury and suggested its favorable therapeutic role for myocardial I/R injury.
微小 RNA（miRNA）被认为在参与心肌缺血/再灌注（I/R）损伤的病理生理学过程中具有重要作用。本研究旨在评估 miR-20a 在心肌 I/R 损伤中的功能意义和潜在的调控机制作用。在模拟 I/R 的心肌细胞缺氧/复氧（H/R）模型中，我们观察到 miR-20a 在经历 H/R 的 H9c2 细胞中减少。miR-20a 模拟物促进心肌细胞活力并减少 H/R 引发的细胞凋亡，而 miR-20a 抑制剂在经历 H/R 损伤的 H9c2 细胞中引起相反的反应。此外，我们确定 TLR4 是 miR-20a 的下游靶基因之一，并揭示 miR-20a 可能通过使 p38 MAPK/JNK 信号失活来发挥其对 H/R 心肌细胞的保护作用。总之，本研究强调了 miR-20a 减轻心肌细胞 H/R 损伤的潜力，并为心肌 I/R 损伤提供了有利的治疗作用。
